In case of serious poisoning and intoxication, the kidneys can be affected primarily with the development of toxic nephropathy. Only timely treatment will help a person avoid the most serious complications of such phenomena - renal failure.

Toxic nephropathy

Toxic nephropathy is understood as damage to the parenchyma of the kidneys, their glomerular apparatus, which occurs against the background of exposure to exogenous and endogenous toxic products and metabolites (ICD-10 code - N14.4).

The classification of pathology includes the following types:

1. Specific nephropathy. It is associated with acute external toxicosis arising from poisoning with various nephrotoxic substances. Often the developing renal dysfunction is preceded by toxicogenic liver damage.
2. Nonspecific nephropathy. It is caused by hemodynamic disorders of various etiologies, provoked by various severe poisoning.

Causes and pathogenesis

Kidney damage can occur due to the pathogenic effect on their tissues of the toxic substances themselves, their decay products, as well as against the background of the development of an autoimmune reaction.

Most often, the disease is caused by such substances:

• Heavy metals, their salts;
• Ethylene glycol;
• Oxalic, acetic acid;
• Pesticides, herbicides;
• Arsenic;
• Solvents;
• Copper sulfate;
• Poisons of animals, insects;
• Mushroom toxins;
• Nitrogen-containing compounds;
• Volatile ethers;
• Low quality alcohol.

Often, toxic nephropathy is recorded in people employed in hazardous industries, where work is associated with poisons, chemicals, rubber, polymers. All substances can enter the body both through the respiratory system, and through the blood, through the skin (with bites).

Sometimes even some medications - antibiotics, NSAIDs - cause toxic nephropathy. Nonspecific kidney damage is possible with myoglobinuria, exotoxic shock, severe disorders of renal trophism in coma, compression of organs.

After exposure to the kidneys toxins and metabolites, edema of parenchymal cells is observed, as well as disruption of the renal glomeruli, which causes disruptions in cellular respiration and leads to the deposition of protein fractions. If the body is affected by hemotoxic poisons, they simultaneously destroy erythrocytes, as a result of which hemoglobin clogs the structural units of the kidneys - nephrons. In some cases, kidney damage occurs against the background of their oppression by free amino acids. Whatever the pathogenesis, ultimately, there is oxygen starvation of the kidney tissue, its ischemia, which, without treatment, leads to tubule and glomerular necrosis.

Symptoms

The severity of organ damage will largely depend on the type of substance that entered the body, on its amount, on the method of ingestion. The health of the urinary system before the onset of pathology also plays a role - in the presence of chronic kidney diseases, nephropathy can develop even from small doses of toxic substances.

The clinical picture resembles that of acute glomerulonephritis. First appear general symptoms - weakness, weakness, lethargy, temperature may rise. Further, the person notes the swelling of the legs, puffiness of the face. The indicators of the composition of urine change - the amount of protein increases in it, blood appears (erythrocytes).

Other common signs of pathology:

• Enhancement blood pressure up to very high numbers.
• Decrease in urine output, frequency of urination (sometimes complete anuria).
• Low back pain due to kidney edema.
• Convulsions.
• Decreased heart rate.
• Arrhythmia.
• Wheezing in the lungs.

Depending on the type of toxic substance to those described above clinical signs specific symptoms may also join. For example, if a person is poisoned by an excessive amount of sulfonamides, then with toxic nephropathy, he has pain in the joints, hemorrhages on the skin and mucous membranes, and a fever.

In terms of severity, the disease is differentiated in this way:

1. The first is a moderate increase in protein, hemoglobin and erythrocytes in the blood, mild symptoms.
2. The second - diuresis falls, the amount of urea, potassium, creatinine in the blood increases greatly, the symptoms increase.
3. Third, due to renal edema and a sharp decrease in glomerular filtration rates, acute renal failure, a deadly complication, may develop.

In the progression of renal failure with toxic nephropathy, several stages are also distinguished:

1. Initial (up to 3 days). The actual poisoning of the body with nephrotoxic agents occurs.
2. Oligoanuric (1-2 weeks). Due to fluid retention, urine excretion decreases, which leads to an overload of the heart and the development of edema, shortness of breath, wheezing in the lungs. At this stage, cerebral edema is also possible. Death occurs from suffocation with pulmonary edema, cardiac arrest, DIC syndrome. Secondary vasculitis, anemia, and thrombocytopenia often join.
3. Stage of polyuria (up to several months and years). This stage occurs with a favorable course of the disease. Diuresis increases, which can also lead to dehydration.
4. Recovery. All indicators of urine and kidney function are normal, but full recovery perhaps not in all patients.

Diagnostics

Usually, diagnostic measures are carried out already in the nephrology department, where a patient is brought with suspicion of acute kidney damage. In addition to the characteristic clinical picture, the doctor pays attention to the history of the pathology, finds out the possible nature of the poisoning.

Examination methods for toxic nephropathy are as follows:

• General analysis of blood, urine;
• Blood test for pH, electrolytes;
• Biochemical blood test in terms of indicators of kidney function;
• Ultrasound of the kidneys;
• If necessary, kidney MRI.

With nephropathy, ESR, the number of leukocytes in the blood most often increase, anemia is observed. The amount of protein, nitrogenous compounds increases in urine, hemoglobin and erythrocytes, cylinders appear. The specific gravity of urine is increased, and creatinine, urea, uric acid, and potassium increase in the peripheral blood.

Treatment

Often, the treatment of toxic nephropathy is carried out in the intensive care unit, especially in acute renal failure. In a less serious state of affairs, treatment is carried out in a standard ward of the department of nephrology (urology). A set of measures to treat the disease should be started immediately, preferably under the supervision of a toxicologist.

The most important are measures to remove toxins and poisons from the body. This is achieved by performing the following techniques:

• Plasmapheresis;
• Hemodialysis;
• Hemofiltration;
• Hemisorption;
• Gastrointestinal lavage.

Forced diuresis is carried out by introducing aminophyllin, mannitol, lasix. To lavage the stomach, vaseline oil or a large amount of liquid is injected into it. Hemodialysis is recommended in the first 6 hours of illness, then peritoneal dialysis (purification of blood through the peritoneum) is performed for another 48 hours.

Of the drugs for toxic renal nephropathy, sorbents, diuretics, glucocorticosteroids, as well as copious alkaline drinks can be recommended. The treatment is supplemented with the administration of glucose with vitamin C, insulin, sodium bicarbonate, calcium chloride, vitamins. If necessary, transfusion of albumin and plasma is performed.

The disease is difficult to treat, since the structure of the kidneys is poorly restored, and the death of nephrons can begin already in the early stages of the development of the disease. As a result, kidney performance is irreversibly impaired. Therefore, it is important to start therapy on the very initial stage disease.

Complications and prognosis

The prognosis for toxic nephropathy depends on the type of poisonous substance and the severity of the course of the disease, mortality ranges from 20-70%. The prognosis is favorable only with the adequacy of therapy and its timeliness. The worst prognosis is when cadmium, silicon, hydrogen arsenate enter the body.

Complications most often develop with a high concentration of toxins and poisons in the body, when they are introduced not through airways, but through the blood. Complications include hemolytic uremic syndrome, interstitial nephritis, and acute renal failure. The latter complication is often fatal due to renal necrosis and complete renal failure.

What is Toxic Nephropathy

Allocate specific kidney damage in acute exotoxicosis. It is associated with poisoning with nephrotoxic substances: ethylene glycol, oxalic acid, mercury, chromium, lead, arsenic. Toxic nephropathy occurs when poisoning with hemolytic substances (acetic acid, arsenous hydrogen, copper sulfate). Renal dysfunction develops following toxic liver damage (hepatorenal syndrome).

Allocate non-specific kidney damage. It manifests itself in severe poisoning with various poisons, as well as in hemodynamic disorder (primary toxicogein collapse, ETS). A large place in the structure of kidney damage is occupied by positional compression syndrome, which is a complication coma.

Pathogenesis (What Happens?) During Toxic Nephropathy

Pathogenesis of toxic nephropathy largely depends on the etiology. When poisoning with ethylene glycol and oxalic acid, it is associated with edema of the nephrons. Specific action salts of mercury is due to the binding of protein sulfhydryl groups, which leads to disruption of cellular respiration of nephrons and protein precipitation. A similar mechanism of action is observed for other heavy metal salts.

In case of poisoning with hemolytic poisons, erythrocytes are destroyed and free hemoglobin is released, which clogs the nephrons. In positional compression syndrome, the nephrons are affected by free myoglobin. Hepatorenal syndrome is caused by toxic kidney damage by free amino acids (leucine, tyrosine, etc.).

All these reasons lead to ischemia of nephron cell membranes. If ischemia continues for several days, irreversible necrobiotic changes occur in the glomeruli and tubules.

Symptoms of Toxic Nephropathy

The clinical picture.There are three degrees of toxic nephropathy:

• Mild degree characterized by the appearance of protein in the urine, shaped elements blood and cylinders.
• Average degree manifests itself, in addition to these symptoms, a decrease in urine output, a moderate increase in urea, creatinine, potassium and other metabolites.
• Severe degree characterized by a picture of acute renal failure (ARF).

Acute renal failure

Allocate the initial, oligoanuric, polyuric phases of acute renal failure and the recovery period.

The initial phase of ARF lasts 1-3 days and is characterized by signs acute poisoning substances with nephrotoxic effects. In these patients, daily monitoring of diuresis is necessary, when it decreases, stimulation is performed with 16% mainit solution, lasix (100-200 mg per injection) in combination with euphyllin.

The oligoanuric phase lasts 7-14 days. This is the most difficult phase of the arrester. It has a decrease in diuresis (less than 500 ml / day oliguria, less than 50 ml / day anuria), fluid retention (acute water poisoning of hydremia) causes overload of the left ventricle, "wet lungs" syndrome, which is accompanied by shortness of breath, the appearance of wet wheezing in the lungs. Pulmonary and cerebral edema may develop. The body accumulates toxins and, above all, products of protein metabolism: creatinine, urea and medium molecules, their level rises 3-4 times after a few days. Weakness, lethargy appear. There may be potassium intoxication, with hyperkalemia of 811 mmol / l, a decrease in the rhythm and even cardiac arrest is observed. The ECG shows a decrease in amplitude complexes QRS, development of sinoauricular, atrioventricular and intraventricular blockages is possible, there is a high-amplitude hyperkalemic T wave with a narrow base.

In this stage, acidosis progresses rapidly, the pH drops to 7.3. Metabolic shifts inhibit hematopoiesis (hemosynthetase), anemia and thrombocytopenia increase, secondary toxic vasculitis joins. All this can lead to bleeding and the development of DIC. Irritation of the bone marrow with toxic substances is accompanied by leukocytosis with a shift of the leukocyte formula to the left.

Polyuric phase. With a favorable course of ARF, the oligoanuric phase passes into the polyuria phase. Diuresis increases and then increases with a low specific gravity of urine. Sometimes it reaches more than 35 l / day. This is due to a violation of the reabsorption of water and salts by the tubules of the idioms. So polyuria can lead to dehydration and hyposalemia. The duration of the polyuria phase is 1530 days.

The recovery period is characterized by a gradual increase in urine specific gravity and normalization of homeostasis. This process lasts from 6 months to 2 years.

Mortality in acute renal failure varies widely (from 20 to 70%) depending on the etiological factor.

Treatment is differentiated into helping the patient in the toxicogein and somatogenic phases of poisoning. In the toxicogein phase, therapeutic measures are aimed at detoxification and prevention of toxic nephropathy. In the somatogenic phase, ARF syndrome is treated. With a decrease in diuresis, it is stimulated with manitol (500 ml of a 16% solution intravenously, 2 times a day) or lasix (100 mg intravenously, 2 times a day). Diuresis increases with intravenous administration aminophylline.

In the phase of oligoanuria, 500 ml of 20% glucose solution with the addition of 5 ml of 5% solution is administered intravenously daily. ascorbic acid and 16 U of insulin to reduce urea and potassium intoxication. In order to eliminate acidosis, 250-500 ml of 4% sodium bicarbonate solution is injected (under control of serum pH). To restore the level of calcium and prevent hemorrhage, a 1% solution of calcium chloride (150 ml) is shown. Recommended transfusion of plasma and albumin, the appointment of vitamin complexes, drugs that improve metabolism (actovegin, solcoseryl, cytochrome, cytomac). Anabolic hormones (hierobol, retabolil) are shown no earlier than a week after poisoning.

An increase in the level of urea to 30-40 mmol / l and potassium more than 67 mmol / l is an indication for hemodialysis. With massive edema, ultrafiltration is performed. Emergence hemorrhagic syndrome and collapse is a contraindication to these treatments. Peritoneal dialysis can be used for detoxification.

Recently, for the same purpose, therapeutic lymphorrhea has been used in an amount of 1000-4000 ml. In the phase of polyuria, it is necessary to monitor the electrolyte balance of the body.

Treatment of Toxic Nephropathy

The first type of measures is etiological treatment, which is of a preventive nature and is most effective if it is used promptly in the first hours of the disease.

Even with severe poisoning with dichloroethane, in the case of very early measures to accelerate the elimination of the poison from the body, the clinical picture of toxic hepatopathy turns out to be more favorable, without the phenomena of liver failure.

In case of poisoning with hepatotoxic substances, the combined use of several treatment measures to remove these substances from the body: early gastric lavage followed by the introduction of vaseline oil or an adsorbent into it ( activated carbon), hemodialysis for 5-6 hours under the control of a decrease in the concentration of these drugs in the blood, peritoneal dialysis for 1-2 days, taking into account the possibility of washing out these compounds from the fat depot of the omentum.

Theoretically, it is quite justified to use a specially prepared sterile oil, for example, interlipid, instead of the usual standard dialysis solution, which significantly increases the clearance of fat-soluble drugs. Rationally simultaneous forced diuresis, better with the use of osmotic diuretics (sorbitol, mannitol). Although the amount of excreted hepatotoxic substances in the urine is small, the use of osmotic diuresis makes it possible to increase the osmosis of the epithelium of the renal tubules to a state of functional hydropia, which reduces the resorptive function of the epithelium and to some extent protects it from gross damage by nephrotoxins or amino acids secreted by the damaged liver, which are normal are deaminated.

Which doctors should you contact if you have Toxic Nephropathy?

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This is damage to the glomerular apparatus and renal tubules, caused by the action of exo- and endotoxins, hemodynamic and metabolic disorders in case of poisoning. Manifested by back pain, asthenic syndrome, edema, oligoanuria, which is subsequently replaced by polyuria, multiple organ disorders. Diagnosed with a general biochemical analyzes blood and urine, samples of Reberg, Zimnitsky, ultrasound and tomography of the kidneys, ultrasound of the renal vessels, chemical and toxicological studies. Treatment includes detoxification therapy, infusion correction of metabolic disorders, RRT.

ICD-10

N14.4 Toxic nephropathy, not elsewhere classified

General information

Toxic nephropathy is a collective term that combines a number of nephrological diseases with similar etiopathogenesis and clinical presentation. The prevalence of pathology reaches 0.04%, which is up to 20% of all reported cases of ARF. The increase in morbidity is associated with the increasing use of chemicals in various industries and in everyday life: according to observations, annually up to 10 million people are constantly in contact with nephrotoxic chemicals. In addition, the downside to the success of the pharmaceutical industry has been the emergence of medicinesaffecting the kidneys. The relevance of the timely detection of the toxic form of nephropathy is due to high level mortality and severe outcomes with irreversible destruction of kidney tissue.

Causes

Damage to the renal parenchyma is caused by exposure to chemicals that have a direct or indirect nephrotoxic effect. In most cases, renal dysfunction, and in severe cases, tissue destruction, is caused by exogenous industrial and household poisons, although in some patients the disease is caused by endogenous intoxication. Specialists in the field of urology and nephrology distinguish the following groups of reasons that lead to the development of nephropathy:

• Taking substances with nephrotoxic effect... When poisons of this group enter the kidneys, acute glomerulopathy or tubular necrosis occurs, caused by the reabsorption of a large amount of toxic substances. Salts of heavy metals (cadmium, lead, mercury, gold, arsenic, iodine, bismuth, chromium, etc.), ethylene glycol, oxalic and others have a direct damaging effect on the renal tissue. boric acid, gasoline, phenol, toluene, orellanin mushroom toxins, poisons of some animals.
• Indirect toxic kidney damage... Poisoning by substances with a hemolytic effect (acetic acid, arsenous hydrogen, copper sulfate, snake venom and others) are complicated by blockage of the nephrons by hemoglobin. Similar damage is caused by massive crushing of tissues and prolonged compression syndrome, in which myoglobinuria is observed. In case of toxic liver damage, the renal parenchyma is secondarily damaged by xenobiotics and endogenous toxins.
• General clinical manifestations of poisoning... A number of chemicals do not have a direct nephrotoxic effect, but the systemic manifestations that occur when they are taken lead to severe renal dysfunction. Most often, toxic forms of nephropathy develop against the background of poisoning with a clinic of shock, uncompensated acidosis, and pronounced metabolic disorders. The same situation arises under the influence of endo- and exotoxins of pathogenic and opportunistic microflora.

Continuous expansion of the range medications, primarily antibacterial and antineoplastic agents, has led to an increase in the incidence of toxic drug nephropathy. Studies have shown that in more than 30% of patients, nonoliguric renal failure is associated with pharmaceuticals.

Pathogenesis

The mechanism of development of toxic nephropathy is determined by the reasons that provoked renal dysfunction. The pathogenesis of disorders caused by direct nephrotoxins is based on the disruption of biochemical processes in the nephrons, epithelial cells of the proximal and distal tubules. After filtration by the glomeruli, the toxic substance enters the tubular system, where, due to the reabsorption of water, its level increases almost 100 times. The resulting concentration gradient contributes to the entry and accumulation of xenobiotics in the tubular epithelium up to a certain critical level.

Depending on the type of exotoxin in epithelial cells, the processes of destruction of cell and mitochondrial membranes, lysosomes, components of the cytoplasm, smooth endoplasmic reticulum, ribosomes, etc. occur, with the development of acute tubular necrosis in the most severe cases. Some nephrotoxins, due to the initiation of hyperimmune processes, destroy the glomerular apparatus of the cortex. The deposition of immune complexes in the glomerular structures or the formation of complex antigens in the membranes, followed by an attack of antibodies, provoke the onset of acute glomerulonephritis or interstitial nephritis without damaging the tubular epithelial cells. An important factor in direct nephrotoxicity is the ability of certain substances to stimulate the formation of free radicals.

The pathogenesis of mediated kidney damage during tubule blockage is based on the development of necrotic processes in their cells, impaired reabsorption capacity. Intrarenal stagnation of urine is accompanied by retrograde flow of glomerular filtrate and subsequent damage to the nephrons. With nephropathies that have arisen against the background of general poisoning, the basis of pathomorphological changes is usually cell ischemia and a violation of biochemical processes due to acid-base and water-electrolyte imbalance. At the initial stage, dysfunction of epithelial cells occurs, which can subsequently be complicated by toxic degeneration and necrosis of tubular epithelium, destruction of glomerular basement membranes, and interstitial edema.

Classification

Systematization of forms of toxic nephropathy is carried out taking into account the peculiarities of the etiopathogenesis of the disease and the severity of symptoms. This approach allows you to develop the optimal tactics for managing the patient, and in some cases, prevent the development of irreversible tissue destruction. Taking into account the etiological factor and the mechanism of kidney damage, the following forms of the disease are distinguished:

• Toxic specific nephropathy... It develops under the influence of exogenous and endogenous substances with direct and indirect nephrotoxic effects. It is characterized by the rapid development of tissue destruction, which is irreversible in some patients. More often requires early initiation of renal replacement therapy.
• Toxic nonspecific nephropathy... Complicates the course of poisoning and diseases with severe intoxication syndrome, in which hemodynamic and metabolic disorders become leading. At the initial stages, violations are of a functional nature, and only later does tissue destruction begin.

With a mild course, nephropathy is detected by laboratory: in a clinical analysis of urine, it is determined increased content protein, leukocytes, erythrocytes, cylinders appear. The average degree is characterized by a decrease in the amount of urine and a violation of the filtration function with an increase in the level of urea, creatinine, potassium in the blood serum. For a severe course, the clinic of acute renal failure is characteristic, up to the onset of uremic coma.

Symptoms of toxic nephropathy

Within 1-3 days after poisoning, clinical symptoms are manifested by a feeling of heaviness, dull aching pains in the lumbar region, general weakness, rapid fatigability. With significant dysfunction and destruction of the kidneys, urine staining with blood (gross hematuria) is possible. From 2-4 days, the volume of diuresis decreases, characteristic "renal" edema appears on the face, which decrease or completely disappear by the end of the day. The patient is constantly thirsty, complains of headache and muscle soreness.

There is nausea, vomiting, diarrhea. Skin and the visible mucous membranes become dry, icteric. The increase in renal failure is accompanied by an almost complete cessation of urination, increased edema, its descending spread to other parts of the body, and the appearance of a petechial rash. With severe lesions, cerebral symptoms develop - lethargy, lethargy, stunnedness, auditory, visual, tactile hallucinations, convulsive syndrome... Signs of severe renal dysfunction usually persist for 7-14 days.

At the next stage of the development of the disease, lasting from 10-15 to 30 days, oligoanuria is replaced by a gradual increase in diuresis. The patient excretes from 1.8 to 5-8 liters or more of urine per day. Weakness, fatigue, excruciating thirst persist, body weight decreases. The duration of the recovery period in intoxication nephropathy depends on the volume and nature of the lesion. Usually, it takes from 6 months to 2 years to restore the functional viability of an organ.

Complications

In 20-70% of cases, toxic nephropathy is fatal due to massive irreversible destruction of the renal parenchyma. A decrease in filtration function in patients with acute renal failure leads to hyperkalemia with a slowing heart rate, fibrillation and ventricular asystole. Cardiac dysfunction in combination with hypoproteinemia increases the risk of pulmonary edema.

Prolonged uremia is accompanied by increased release of nitrogenous metabolites through the skin, serous and mucous membranes with the development of uremic pericarditis, pleurisy, gastritis, enterocolitis, laryngotracheitis, toxic damage to the liver, bone marrow. If the secretion of the components of the renin-angiotensin system is disturbed, the development of arterial hypertension is possible. Long-term consequences of toxic kidney damage are chronic tubulo-interstitial nephritis, chronic renal failure, neoplasms of the urinary tract.

Diagnostics

Diagnosis of toxic nephropathy is usually straightforward in cases where the disease arose after chemical poisoning. Diagnostic search is aimed at assessing the nature, volume of possible tissue damage, determining the severity of renal dysfunction. The following laboratory and instrumental research methods are recommended for patients with nephropathy:

• General urine analysis... Proteinuria, leukocyturia, microhematuria, cylindruria are determined. The relative density of urine in the oligoanuric phase exceeds 1030 g / l, in the polyuric phase it is below 1003 g / l. Additional testing of Zimnitsky for polyuria reveals a decrease in the concentration function.
• Blood chemistry... Until the volume of diuresis is restored, serum levels of creatinine, uric acid, urea nitrogen, potassium, calcium, and inorganic phosphorus increase. Violation of the filtration capacity of glomeruli is also confirmed by the results of the nephrological complex and Reberg's test.
• Kidney ultrasound... On ultrasound, toxic nephropathy is manifested by an increase in the size of the renal parenchyma due to interstitial and lymphostatic edema. Areas of necrosis look like hypoechoic cavities or hyperechoic inclusions. Doppler ultrasonography of the renal vessels reveals hemodynamic disorders.
• Kidney tomography... Computed tomography of the kidneys allows you to obtain a layer-by-layer image of the renal tissue and detect even small areas of destruction. For safety reasons in toxic lesions, the study is recommended to be carried out without contrast or to replace it with MRI, although in this case the information content is somewhat reduced.

To confirm the toxic nature of nephrological pathology, chemical and toxicological studies are carried out, if possible, to establish the chemical that caused the disorder. Contrast methods studies (excretory urography, renal angiography) are used with caution due to the risk of aggravating the clinical situation by contrast-induced destructive processes. To monitor the state of other organs and systems, biochemical liver tests, coagulogram, ECG are carried out. Changes general analysis blood levels are nonspecific: anemia, moderate leukocytosis, increased ESR, thrombocytopenia can be detected.

Nephropathy of toxic origin is differentiated with secondary nephropathies of another genesis (contrast-induced, diabetic, dysmetabolic, etc.), acute glomerulonephritis, ischemic necrosis of the kidneys, traumatic damage to the renal parenchyma, atheroembolic disease. At the appointment of a urologist-nephrologist, the patient is consulted by a toxicologist, anesthesiologist-resuscitator, neurologist, therapist, cardiologist, pulmonologist, hepatologist.

Treatment of toxic nephropathy

Patients whose kidneys are damaged as a result of poisoning with exo- or endotoxins are hospitalized in the intensive care unit. The main therapeutic objectives are the prompt elimination of the chemical, the correction of metabolic disorders, the prevention possible complications... Taking into account the stage of the disease, patients are shown:

• Detoxification therapy... It is carried out in the first hours and days after poisoning. For the accelerated elimination of the toxin, gastric lavage, forced diuresis with the appointment of osmotic diuretics and saluretics are carried out, adsorbents, laxatives, and specific antidotes are used. In difficult cases, hemosorption, hemofiltration, ultrafiltration, hemodialysis, peritoneal dialysis are effective. Some patients are prescribed transfusions of blood and blood components.
• Infusion correction of metabolic disorders... It begins immediately after hospitalization and continues in the oligoanuric period of acute renal failure. Recovery electrolyte balance and acid-base balance, potassium antagonists (usually calcium preparations), glucose infusion with insulin, alkalizing polyionic solutions are used. Further intake of enterosorbents that bind toxic metabolites is possible. With significant renal dysfunction, RRT is warranted.

With an aggravation of the patient's condition, complex anti-shock therapy is carried out, urgent conditions are stopped (uremic coma, pulmonary edema, convulsive syndrome, hypertensive crisis). In the polyuric phase, massive continues (up to 5-6 l / day) infusion therapy to maintain the BCC and the physiological concentration of metabolites. At the stage of recovery, restorative treatment is carried out and the tactics of further management of the patient is determined, taking into account the degree of preservation of renal functions.

Forecast and prevention

Toxic nephropathy is a severe, prognostically unfavorable disorder with high mortality rates. Timely determination of the toxin, correct assessment of the morphological preservation and functional viability of the renal parenchyma, and adequate intensive therapy increase the chances of a favorable outcome of nephropathy. Prevention of the disease is aimed at preventing the ingress of toxic substances into the body: limiting the time of contact with nephrotoxic poisons, using personal protective equipment (respirators, protective clothing), refusing to eat unfamiliar mushrooms.

Employees of enterprises with harmful production conditions are recommended to undergo preventive medical examinations for the early detection of renal dysfunction. To reduce the number of cases of hemodynamic and metabolic damage to renal cells in systemic disorders, patients with poisoning are recommended to regularly monitor the functional capacity of the kidneys and adequate relief of the acute condition. Taking into account the growing prevalence of drug nephropathies when prescribing nephrotoxic drugs, a thorough examination of the patient is necessary to identify the prerequisites for toxic damage to the renal parenchyma.

May 8, 2017 Vrach

Toxic nephropathy is a disease that occurs against the background of the effects of various poisons on the human body. There are mild, moderate and severe forms of the disease. Chronic disease can provoke the development of this form of nephropathy ( diabetes) or any infection.

Toxic nephropathy can be specific and non-specific. In the first case, the disease develops when the body comes into contact with poisons that are dangerous to the kidney tissue. The following substances can lead to its development:

1. acetic acid, arsenous hydrogen, copper sulfate provoke the blockage of nephrons with hemoglobin during the destruction of erythrocytes;
2. arsenic, mercury, lead, chromium, oxalic acid, ethylene glycol, when ingested, begin to destroy renal tissue;
3. hepatorenal syndrome, which develops with liver poisoning and is accompanied by the release of amino acids that damage the kidneys.

Nonspecific nephropathy manifests itself when the body comes into contact with poisons that do not directly affect the renal tissue, but lead to its damage. They can provoke a sharp drop in blood pressure, changes in electrolyte balance, local disturbances in blood flow and an uncompensated shift in the acid-base balance towards a decrease in pH. Separately, it is worth mentioning the formation of toxic nephropathy after receiving a compression injury or rupture of muscle tissue. It develops when the kidneys are in a pinched state and cannot remove toxic substances produced by the body.

Infectious toxic nephropathy appears against the background of acute respiratory infections, acute respiratory viral infections and other colds. Children get sick with it more often than adults, because their the immune system growing organism is weaker. The course of this form of the disease is favorable and it does not require specific and therapeutic measures. As the infectious process is eliminated, nephropathy goes away. The manifestation of the disease disappears completely in 3-4 weeks.

Causes

The disease appears due to exposure to poisons, breakdown products of chemicals or an autoimmune reaction caused by poisoning of the body. The degree of damage to the renal tissue depends on the amount of penetrated substances, the way they enter the body and chemical composition... Another factor affecting the development of the disease is the condition genitourinary system... People with chronic pyelonephritis, ICD, nephroptosis, glomerulonephritis are more difficult to tolerate the effects of toxic substances on the kidneys. Toxic type nephropathy most often develops due to:

1. unauthorized use of medications (anti-inflammatory drugs, antibiotics);
2. penetration of salts of heavy metals into the body;
3. contact with organic solvents or pesticides;
4. penetration of exogenous chemical compounds (fungal toxins, bite of a tick or other insect, animal).

Disease manifestations

The symptoms of the disease are varied and often correspond to renal failure, which complicates the diagnostic process. The first manifestation of the disease is considered to be a change in the composition of urine during OAM. Many patients are admitted to hospitals with medication-related nephropathy. Intoxication leads to the formation of a specific autoimmune reaction. The manifestations are as follows:

• increased blood pressure;
• lower back pain;
• swelling of the limbs and face;
• decrease in the amount of urine excreted;
• the appearance of blood in the urine or protein;
• convulsions.

Depending on the type of drug that caused the poisoning, specific signs of intoxication may appear. Renal failure is a serious complication of nephropathy. If you do not go to the hospital in time, a person may fall into a coma.

Diagnostics

A biochemical and clinical blood test allows you to identify the presence of a disease in the body. Additionally, the following research methods are used for diagnosis:

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• general urine analysis;
• Ultrasound of the kidneys;
• check water balance organism;
• diuresis accounting.

Features of therapy

Nephropathy is treated in a hospital. If a patient is admitted in a serious condition, then he is left in intensive care. The first stage in stabilizing the patient's condition is removing the toxin from the body. If the cause is an autoimmune reaction, then corticosteroids are used to reduce the manifestations of allergies. Doctors carry out the following activities:

• blood purification through special filters;
• the introduction of anti-shock drugs;
• gastric lavage (if the toxin is ingested with food);
• connecting the patient to a device that acts as an artificial kidney;
• acceleration of diuresis by administering diuretics to the patient.

The patient is given diuretics, alkaline drinks, sorbents. During your hospital stay, you must adhere to bed rest. High protein foods should be removed from the diet. If uremia is severe, the patient is transferred to a carbohydrate diet. If the excretory function of the kidneys is not affected, the patient is prescribed an abundant drink.

Doctors monitor the condition of the skin, as toxic products can be released through it. As a result, patients develop severe itching. To avoid this, it is recommended to take a shower or do rubdowns at least 1 time per day. During vomiting, patients are given salty food to reduce the loss of sodium chloride.

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Toxic nephropathy - pathological condition, which is characterized by damage to kidney tissue and impaired function as a result of exposure to toxic substances.

They are of great importance in the processes of biotransformation of most toxins. It is the kidneys that take an active part in their metabolism and elimination from the body. This is accomplished through the processes of filtration, secretion and excretion through the functioning of complex transfer systems. Kidneys are able to excrete water-insoluble chemical substances, while their concentration in the structures of this organ is much higher than that in the blood serum.

The involvement of the kidneys in the elimination of toxins creates conditions for prolonged contact with these substances, which increases the likelihood of developing nephropathy.

Causes of occurrence

Some medications (in particular, NSAIDs, antibiotics, cytostatics, and others) can cause toxic nephropathy.

Any exogenous chemical or biological substance can cause kidney damage. However, some of them have a special affinity for the renal tissue and, more often than others, negatively affect the renal structures. They are called "nephrotoxic substances". Among them, the most common nephrotoxic factors are:

• medications (antibiotics, and sulfa drugs, anticonvulsants and cytostatics);
• x-ray contrast agents;
• excess of the concentration of substances existing in the human body under physiological conditions (uric acid, potassium, calcium);
• compounds of heavy metals (lead, arsenic, mercury, cadmium, beryllium, bismuth, etc.);
• chemical agents used to combat pests and plant diseases (phosphorus compounds, chlorinated hydrocarbons);
• organic solvents (tetrachlorethylene, methanol, carbon tetrachloride);
• glycols;
• hemolysins, etc.

The mechanisms of development of toxic nephropathy can be different:

• direct damaging effect due to its own high toxicity;
• negative impact due to exceeding the permissible concentrations;
• allergic reactions.

The nature and extent of kidney damage depend not only on the chemical composition of the toxin and its concentration, but also on the initial state of the organ. The kidneys, in which a pathological process already exists, is much more difficult to tolerate the effects of toxic substances, even in low concentrations.

How does it manifest

The clinical manifestations of toxic nephropathy are diverse. Relatively mild forms of the disease with predominantly laboratory changes (and protein in the urine) are more common. However, with prolonged exposure to high concentrations of toxins or with reduced reactivity of the body and the presence of a background disease, severe and irreversible kidney damage is possible.

Particular attention should be paid to drug nephropathies, as their prevalence is increasing every year. Unlike other types of toxic kidney damage in drug nephropathy, not only the toxic component is important, but also allergic reactions. Due to the abundant blood supply to the kidneys, allergic phenomena have a severe course with damage vascular system and interstitium.

Medicinal kidney damage can occur:

• sharp;
• nephrotic syndrome;
• tubulointerstitial nephritis (s);
• retroperitoneal fibrosis;
• education.

Acute drug glomerulonephritis often develops against the background of general manifestations of allergy and can complicate the course of serum sickness. It usually presents with one of the following syndromes:

• nephrotic (massive proteinuria, edema, decreased level total protein and albumin in the blood, hypercholesterolemia);
• (hematuria, proteinuria, arterial hypertension, edema).

The combination of glomerulonephritis with arthralgia, severe skin lesions, high fever is characteristic of sulfanilamide nephropathy. This pathology is based on necrotizing lesion of small renal vessels.

Severe forms of toxic kidney damage with acute renal failure can be caused by:

• acute tubular necrosis;
• bilateral cortical necrosis;
• acute lesion of tubulointerstitium;
• hemolyticouremic syndrome;

Acute tubular necrosis often develops as a result of the introduction of radiopaque substances (urografin, verografin) into the body during diagnostic procedures, since the latter are deposited in the renal tubules, forming precipitates and causing their obstruction. Contribute to this:

• the introduction of too large doses of contrast;
• decreased filtration capacity of the kidneys against the background of heart failure, diabetes mellitus;
• conducting research on the background of dehydration.

Such kidney damage is characterized by a rapid increase in uremia and a poor prognosis.

Also, acute tubular nephrosis can be caused by taking aminoglycoside antibiotics. It is often combined with hearing loss (due to ototoxicity) and manifests itself:

• oliguria (decrease in the amount of urine excreted);
• a decrease in the relative density of urine;
• slight proteinuria and hematuria.

One of the most frequent reasons development of acute renal failure with drug-induced renal lesions is acute tubulointerstitial nephritis. It is characterized by:

• dull pain in the lumbar region;
• an increase in the daily amount of urine;
• changes in urinary sediment (presence of protein and leukocytes);
• early renal dysfunction with an increase in azotemia without oliguria.

Rare complications of drug nephropathy include bilateral cortical necrosis. It has a severe course and is clinically manifested:

• oliguria;
• an increase in the content of nitrogen metabolism products in the blood;
• fever;
• intense back pain;
• massive excretion of protein and erythrocytes in the urine.

Hemolytic uremic syndrome complicates therapy with cytostatics. The main clinical manifestations this pathology can be:

• progressive uremia.

Against the background of taking non-steroidal anti-inflammatory drugs, hepato-renal syndrome often develops. A distinctive feature of this pathology is the preservation of the concentration function of the kidneys with a rapid decrease in their ability to filter. Typical signs of this disease are:

• decrease in the daily amount of urine;
• hepatocellular failure;
• rapidly increasing azotemia.

In case of poisoning with nephrotoxic poisons, the patient develops a picture of acute renal failure against the background of symptoms of general intoxication and toxic intestinal damage.

Basics of diagnosis and treatment

In difficult diagnostic situations, a kidney biopsy is performed.

Diagnosis of toxic nephropathies is a rather difficult task for a doctor. In order to make a correct diagnosis, it is necessary to compare the clinical and laboratory data, as well as to identify a possible toxic effect in the anamnesis. The survey plan in such cases includes:

• ultrasound examination of the kidneys;
• in difficult cases -.

The main principle of the treatment of toxic kidney damage is to eliminate their cause, namely, to stop the effect of a toxic substance and remove it from the body. In the future, the tactics of managing patients depends on the nature and severity of pathological changes.

• Methods are used to eliminate antigen.
• For acute damage to the renal glomeruli or interstitial tissue, corticosteroids are prescribed.
• For hemolytic uremic syndrome, they are used